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2014 Mechanisms of Cancer Prezi

Cell cycle, check points, checkpoint failure and cancer.
by

Luke De

on 13 November 2014

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Transcript of 2014 Mechanisms of Cancer Prezi

Welcome to the Cell Cycle (Mitotic/Asexual)
I hope that you can appreciate this as much as I do. Realize that from the knowledge of this process you can begin to evaluate drug therapies that you have.

As Sun Tzu says, "Know thyself and know thy enemy and you will win a thousand battles"

Unfortunately the brilliant and beautiful aspect of this disease that makes it so dangerous is this. In the case of cancer thyself and thy enemy are the same.
This prezi is currently under construction.
Do not print it at this time.
Created by Luke De
Simple
Created by Luke De
Simple
Created by Luke De
Created by Luke De
You ARE the next resource in the battle against cancer. (Sun Tzu)
Created by Luke De
Created by Luke De
Arganine
One of the most common mutations found in the p53 of cancer patients is Arg 248,
Why might this be, and what type of mutation would be the most dangerous?
Created by Luke De
G1 (gap 1)
Synthesis 12hr
(replication)
G2 (Gap2)
Nuclear Division 1hr
(Mitosis)
Cytokinesis
Mitogen
(Start signal)
Opportunistic
Go
Phases of the
Cell Cycle
Starting The Process—turning on the switch:
External Signal e.g. Mitogen
Two Methods of Control:
Genetic Regulation
Regulating experssion
of vital genes e.g. operons
Specific cyclins are transcribed in response to specific regulatory factors




Enzyme Regulation
Activating or inactivating
regulatory enzymes
Activated by cyclins
Transcription Video
Expression
missing TF
with Transcription Factors
Replication
Telomeric Replication
The Ground-Breaking Experiments
Overview Videos
Cell division and the Cell Cycle
Epigenetics Review
Apoptosis
?
S-CDK
Rankin, S., Ayad, N. G., & Kirschner, M. W. (2005). Sororin, a Substrate of the
    Anaphase-Promoting Complex, is Required for Sister Chromatid Cohesion in
    Vertebrates. [Abstract]. Mol Cell, (April).
Schmitz, J., Watrin, E., Lénárt, P., Mechtler, K., & Peters, J. M. (2007).
    Sororin is required for stable binding of cohesin to chromatin and for
    sister chromatid cohesion in interphase [Abstract]. Curr Biol, (April).
Zhang, N., & Pati, D. (2012). Sororin is a Master Regulator of Sister Chromatid
    Cohesion and Separation. [Abstract]. Cell Cycle, (June).
Citations:
Dreier, M. R., Bekier, M. E., 111, & Taylor, W. R. (2011). Regulation of sororin
    by cdk1-mediated phosphorylation [Abstract]. J Cell ScI, (September).
Peters, J. M., & Nishiyama, T. (2012). Sister chromatid cohesion [Abstract].
    Cold Spring Harb Perspect Biol, (October).
How does M-Cyclin activate cohesin?
Chartouni, Jiang, Rothpletz, and Teng
M cyclin CDK complex phosphorylates sororin in mitosis activating sororin
Active Wapl keeps cohensions from binding to DNA
Activated sororin will inhibit Wapl allowing cohesins to lock onto DNA.
Citations:
Hirano, T. (2009). Let's play polo in the field of condensation [Abstract]. Mol Cell.
Simpson-Lavy, K., & Brandeis, M. (2011). Phosphorylation of Cdc5 regulates its accumulation
   [Abstract]. Cell Div.
St-Pierre, J., Douziech, M., Bazile, F., Pascariu, M., Bonneil, E., Sauvé, V., . . . D'Amours, D.
   (2009). Polo kinase regulates mitotic chromosome condensation by hyperactivation of condensin
   DNA supercoiling activity. [Abstract]. Mol Cell.
How does M-Cyclin activate condensin?

M cyclin CDK complex phosphorylates Cdc5 which phosphorylates condensin which will keep the sister chromatids condensed.
Production of M-Cyclin
M-Cdk is activated by higher M-Cyclin levels (during G2 and M)
M-Cyclin is produced in G2
E2F is removed when Rb is
dephosphorylated and E2F
is inhibited
M-Cyclin’s gene is transcribed in S
When E2F is binded to the
E2F box on the M-Cyclin
Gene, transcription of
M-Cyclin is inhibited
*Cdks exist throughout the
whole cell cycle*

(P53 must be
phosphorylated twice in
order to become active)
P53
ATM phosphorylates
DNA Damage

Ionizing radiation (double strand break) activates MRN and MRN gets phosphorylated

MRN complex attaches to DNA strand breaks
MRN complex is attached to ATM

MRN recruits ATM and ATM gets phosphorylated
DNA Damage activates P53
Gamma-H2AX
Gamma-H2AX activates BRCT domain
BRCT domain recruits CHK2
CHK2 gets phosphrylated by ATM
CHK2 phosphorylates P53
Myc
Brust-Mascher, I., & Scholey, J. M. (2011). Mitotic motors and chromosome segregation: the mechanism of anaphase b. . Biochemical Society Transactions,39(5), 1149-53. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21936780
Reese, L., Melbinger, A., & Frey, E. (2011). Crowding of molecular motors determines microtubule depolymerization. Biophysical Journal, 101(9), 2190-2200. Retrieved from http://www.sciencedirect.com/science/article/pii/S0006349511010630
Occurs during Anaphase
Divided into two parts: Anaphase A+B
Anaphase A: Kinesin 8+15 (Motor Proteins) depolymerize microtubules at the positive end (microtubule catastrophe)
Microtubules unwind and chromosomes move towards poles
Anaphase B: M-Cyclin is degraded, negative ends of microtubules are inhibited, positive ends are exposed, MTOCS move to opposite ends of the pole because of repulsion.
Chromosomal Segregation
Myc
Cargnello, M., & Roux, P. P. (2011). Activation and function of the mapks and their substrates, the mapk-activated protein kinases. Microbiology and Molecular Biology Reviews, 75(1), 50-83. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063353/

Whisenant, T. C., Ho, D. T., Benz , R. W., Rogers, J. S., Kaake, R. M., Gordon, E. A., Huang, L., & Baldi, P. (2010). Computational prediction and experimental verification of new map kinase docking sites and substrates including gli transcription factors . PLoS Computational Biology,6(8), Retrieved from http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1000908
Mitogen
Receptor
Map KKK
Map KK
Map Kinase
Myc
Transcription
Mitogen to Myc Pathway
Diana Masch, Dana Wang,
Christina Ou, Hunter Conti,
Peter Shim ('15)
Diana Masch, Dana Wang,
Christina Ou, Hunter Conti,
Peter Shim ('15)
Full transcript